Combined impact of summer NAO and northern Russian shortwave cloud radiative effect on Eurasian atmospheric circulation

Based on ERA-Interim and CERES_SYN1deg Ed4.1 datasets, the combined influence of summer North Atlantic Oscillation (SNAO) and positive shortwave cloud radiative effect (SWCRE) events in northern Russia on Eurasian atmospheric circulation is investigated at the intraseasonal scale. The impact of the SNAO on the position of the North Atlantic storm track is modified combined with the Ural anticyclone anomaly contributed by positive northern Russian SWCRE anomalies, which could affect the summer stationary wave pattern. During positive northern Russian SWCRE events under SNAO+, the upstream wave train enhanced by the southward Ural anticyclone anomaly is easily trapped by the northward South Asian jets, thus propagating to low latitudes and causing extreme heat events in East Asia. Under SNAO-, the wave train propagates in the British–Baikal Corridor pattern along polar front jet towards the Far East, slowing down the dramatic melting of sea ice in the Laptev and East Siberian seas. Summer positive SWCRE events in northern Russian act as a bridge by promoting the emergence of the Ural anticyclone anomaly, influencing extreme weather in East Asia and Arctic sea ice variability

Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes

AbstractRheumatoid arthritis (RA) is a chronic joint inflammatory disease that is closely associated with dysregulation of fibroblast-like synoviocytes (FLSs). Protocatechuic acid (PCA), a phenolic compound of anthocyanins, has been proven to possess anti-inflammatory activity. However, the role of PCA in RA has not been investigated. In the present study, we aimed to explore the effects of PCA on the RA-FLSs. The results showed that PCA suppressed the proliferation, invasion, and migration of RA-FLSs in a dose-dependent manner. PCA treatment also inhibited the expressions of matrix metalloproteinase (MMP)-3 and MMP-13, as well as the secretion of inflammatory cytokines including TNF-α, IL-1β, IL-6 in RA-FLSs. Moreover, cell apoptosis of RA-FLSs was significantly induced by PCA treatment. PCA was found to repress the activation of NF-κB signalling, which was evidenced by the decreased expression of p-p65 and increased expression of IκBα. Furthermore, PCA significantly decreased the phosphorylation levels of Akt and mTOR in RA-FLSs. In conclusion, the results indicated that PCA exhibited an inhibitory effect on RA-FLSs via inhibiting the NF-κB and Akt/mTOR signalling pathways. These findings supported the concept that PCA might be a therapeutic agent for RA treatment

Subsampling Spectral Clustering for Large-Scale Social Networks

Online social network platforms such as Twitter and Sina Weibo have been extremely popular over the past 20 years. Identifying the network community of a social platform is essential to exploring and understanding the users' interests. However, the rapid development of science and technology has generated large amounts of social network data, creating great computational challenges for community detection in large-scale social networks. Here, we propose a novel subsampling spectral clustering algorithm to identify community structures in large-scale social networks with limited computing resources. More precisely, spectral clustering is conducted using only the information of a small subsample of the network nodes, resulting in a huge reduction in computational time. As a result, for large-scale datasets, the method can be realized even using a personal computer. Specifically, we introduce two different sampling techniques, namely simple random subsampling and degree corrected subsampling. The methodology is applied to the dataset collected from Sina Weibo, which is one of the largest Twitter-type social network platforms in China. Our method can very effectively identify the community structure of registered users. This community structure information can be applied to help Sina Weibo promote advertisements to target users and increase user activity

SMYD2 Promotes Hepatocellular Carcinoma Progression by Reprogramming Glutamine Metabolism via c-Myc/GLS1 Axis

Metabolic reprogramming, such as alterations in glutamine metabolism or glycolysis, is the hallmark of hepatocellular carcinoma (HCC). However, the underlying mechanisms are still incompletely elucidated. Previous studies have identified that methyltransferase SET and MYND domain-containing protein 2(SMYD2) is responsible for the pathogenesis of numerous types of cancer. Here, we innovatively uncover how SMYD2 regulates glutamine metabolism in HCC cells and promotes HCC progression. We identified that SMYD2 expression is upregulated in HCC tissues, which correlates with unfavorable clinical outcomes. Our in vitro and in vivo results showed that the depletion of SMYD2 inhibits HCC cell growth. Mechanistically, c-Myc methylation by SMYD2 increases its protein stability through the ubiquitin–proteasome system. We showed SMYD2 depletion destabilized c-Myc protein by increasing the conjugated K48-linked polyubiquitin chain. SMYD2 increased c-Myc expression and further upregulated glutaminase1 (GLS1), a crucial enzyme that catalyzes the conversion of glutamine to glutamic acid, in HCC cells. GLS1 plays an important role in SMYD2-mediated HCC progression and glutamine metabolism regulation. The knockdown of SMYD2 inhibited glutamine metabolism in HCC cells and overcame their chemoresistance to sorafenib. Collectively, our findings demonstrated a novel mechanism of how SMYD2 promotes HCC progression by regulating glutamine metabolism through the c-Myc/GLS1signaling, implicating the therapeutic potential of targeting SMYD2 in HCC patients

SMYD2 Promotes Hepatocellular Carcinoma Progression by Reprogramming Glutamine Metabolism via c-Myc/GLS1 Axis

Metabolic reprogramming, such as alterations in glutamine metabolism or glycolysis, is the hallmark of hepatocellular carcinoma (HCC). However, the underlying mechanisms are still incompletely elucidated. Previous studies have identified that methyltransferase SET and MYND domain-containing protein 2(SMYD2) is responsible for the pathogenesis of numerous types of cancer. Here, we innovatively uncover how SMYD2 regulates glutamine metabolism in HCC cells and promotes HCC progression. We identified that SMYD2 expression is upregulated in HCC tissues, which correlates with unfavorable clinical outcomes. Our in vitro and in vivo results showed that the depletion of SMYD2 inhibits HCC cell growth. Mechanistically, c-Myc methylation by SMYD2 increases its protein stability through the ubiquitin–proteasome system. We showed SMYD2 depletion destabilized c-Myc protein by increasing the conjugated K48-linked polyubiquitin chain. SMYD2 increased c-Myc expression and further upregulated glutaminase1 (GLS1), a crucial enzyme that catalyzes the conversion of glutamine to glutamic acid, in HCC cells. GLS1 plays an important role in SMYD2-mediated HCC progression and glutamine metabolism regulation. The knockdown of SMYD2 inhibited glutamine metabolism in HCC cells and overcame their chemoresistance to sorafenib. Collectively, our findings demonstrated a novel mechanism of how SMYD2 promotes HCC progression by regulating glutamine metabolism through the c-Myc/GLS1signaling, implicating the therapeutic potential of targeting SMYD2 in HCC patients